S377 Chapter 18

Mikki M
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Mikki M
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Quiz based on the summaries of Chapter 18
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Question 1

Question
Most types of molecule and cellular component of animal cells are affected during [blank_start]ageing[blank_end], and different types of animal cells have [blank_start]different lifespans[blank_end].
Answer
  • ageing
  • different lifespans

Question 2

Question
Cellular ageing is studied using cells from model organisms that have very different lifespans.
Answer
  • True
  • False

Question 3

Question
Two of the many theories of ageing are the n[blank_start]etwork theory[blank_end], which states that cellular ageing is the result of a [blank_start]combination of processes[blank_end], and the f[blank_start]ree radical theory[blank_end], according to which [blank_start]free radical damage[blank_end] is the cause of [blank_start]molecular and cellular ageing[blank_end].
Answer
  • etwork theory
  • combination of processes
  • ree radical theory
  • free radical damage
  • molecular and cellular ageing

Question 4

Question
Genes that confer protection against [blank_start]free radicals[blank_end] and other stresses may have a positive effect against molecular and cellular damage occurring during [blank_start]ageing[blank_end], but will only be selected for by evolution if they also promote [blank_start]reproductory fitness[blank_end].
Answer
  • free radicals
  • ageing
  • reproductory fitness

Question 5

Question
Vertebrate tissues have a mixture of [blank_start]post-mitotic[blank_end] non-dividing cells, such as [blank_start]neurons[blank_end] and skeletal muscle cells, and [blank_start]dividing[blank_end] cells, such as [blank_start]epithelial cells[blank_end] (and germ cells).
Answer
  • post-mitotic
  • neurons
  • epithelial cells
  • dividing

Question 6

Question
Label the diagram of formation of Reactive Oxygen Species during oxidative phosphorylation at the mitochondria
Answer
  • electron transport chain
  • e-
  • O2
  • O2•-
  • H2O2
  • catalase
  • H2O + O2
  • superoxide dismututase

Question 7

Question
Free [blank_start]radicals[blank_end] are atoms or molecules that possess [blank_start]unpaired[blank_end] electrons and are therefore very [blank_start]reactive[blank_end].
Answer
  • radicals
  • unpaired
  • reactive
  • unreactive

Question 8

Question
There are many naturally occurring [blank_start]free radicals[blank_end]; one major source within cells is [blank_start]oxidative phosphorylation[blank_end], which takes place in the inner [blank_start]mitochondrial[blank_end] membrane.
Answer
  • free radicals
  • oxidative phosphorylation
  • mitochondrial
  • cell

Question 9

Question
Free radicals cause [blank_start]oxidative[blank_end] damage to all types of molecules and cell organelles. Particularly: DNA damage - [blank_start]double strand breaks[blank_end] and altered bases/nucleosides, chain reactions of free radical formation in [blank_start]lipid peroxidation[blank_end], damage to amino acids causing changes to [blank_start]activity/conformation[blank_end] of the protein.
Answer
  • oxidative
  • double strand breaks
  • lipid peroxidation
  • activity/conformation

Question 10

Question
Cellular defences against free radicals have evolved; these are either primary or secondary defences. Primary defences include small-molecule radical [blank_start]scavengers[blank_end], proteins that bind [blank_start]metal ions[blank_end], and [blank_start]antioxidant enzymes[blank_end]. Secondary defences include [blank_start]repair enzymes[blank_end], [blank_start]stress response[blank_end] proteins and [blank_start]protein degradation[blank_end] systems.
Answer
  • scavengers
  • metal ions
  • antioxidant enzymes
  • repair enzymes
  • stress response
  • protein degradation

Question 11

Question
[blank_start]Replicative senescence[blank_end] is the irreversible state reached by proliferative cells when they withdraw from the [blank_start]cell cycle[blank_end], and do not undergo any further divisions. It has been studied by measuring [blank_start]population doublings[blank_end] of cells in culture.
Answer
  • Replicative senescence
  • cell cycle
  • population doublings

Question 12

Question
Senescent cells exhibit changes in [blank_start]gene expression[blank_end], which may not only affect their function, but may also affect [blank_start]surrounding cells[blank_end]. They also look different from [blank_start]dividing cells[blank_end], being bigger and having larger nuclei.
Answer
  • gene expression
  • surrounding cells
  • dividing cells

Question 13

Question
Several different events can cause cells to become [blank_start]senescent[blank_end]; these include [blank_start]telomere[blank_end] shortening, some types of DNA [blank_start]damage[blank_end], decondensation of [blank_start]chromatin[blank_end], overactivity of some [blank_start]mitogenic stimuli[blank_end] and activation of some [blank_start]oncogenes[blank_end].
Answer
  • senescent
  • telomere
  • damage
  • chromatin
  • mitogenic stimuli
  • oncogenes

Question 14

Question
[blank_start]Telomeres[blank_end] may be preferentially susceptible to [blank_start]DNA damage[blank_end], and therefore not only trigger [blank_start]replicative senescence[blank_end] due to [blank_start]shortening[blank_end] caused by repeated cell division, but also act as a type of ‘sensor’ of DNA damaging events, such as [blank_start]oxidative stress[blank_end].
Answer
  • Telomeres
  • DNA damage
  • replicative senescence
  • shortening
  • oxidative stress

Question 15

Question
[blank_start]Post-mitotic[blank_end] cells such as [blank_start]neurons[blank_end] and skeletal muscle cells exhibit a number of changes during ageing. These changes include [blank_start]mitochondrial damage[blank_end], abnormalities in [blank_start]protein folding[blank_end], protein [blank_start]accumulation[blank_end], and [blank_start]protein[blank_end] glycation.
Answer
  • Post-mitotic
  • neurons
  • mitochondrial damage
  • protein folding
  • accumulation
  • protein

Question 16

Question
[blank_start]Mitochondrial[blank_end] function is impaired with age, and genes encoded by [blank_start]mtDNA[blank_end] are particularly vulnerable to [blank_start]oxidative damage[blank_end].
Answer
  • Mitochondrial
  • mtDNA
  • oxidative damage

Question 17

Question
Changes in protein [blank_start]folding[blank_end] and turnover occur with increasing age. perhaps due to problems with [blank_start]chaperones[blank_end] or the protein [blank_start]degradation[blank_end] system. Accumulation of misfolded or [blank_start]damaged[blank_end] proteins therefore often occurs in long-lived cells such as [blank_start]neurons[blank_end]. These can form insoluble [blank_start]aggregates[blank_end] called [blank_start]amyloid[blank_end] fibrils or plaques, causing [blank_start]disease[blank_end].
Answer
  • folding
  • chaperones
  • degradation
  • damaged
  • neurons
  • aggregates
  • amyloid
  • disease

Question 18

Question
Interaction of [blank_start]sugars[blank_end] with amino acid residues starts a series of reactions leading to [blank_start]protein glycation[blank_end] and the accumulation of [blank_start]AGEs[blank_end] (Advanced Glycosylation End-products). Long-lived proteins (e.g. [blank_start]extracellular matrix proteins[blank_end]) are particularly susceptible to damage by [blank_start]glycation[blank_end].
Answer
  • sugars
  • protein glycation
  • AGEs
  • extracellular matrix proteins
  • glycation

Question 19

Question
Both mitotic and post-mitotic cells can be affected by genomic instability.
Answer
  • True
  • False

Question 20

Question
Many segmental [blank_start]progeroid[blank_end] syndromes in humans are due to [blank_start]mutations[blank_end] in genes encoding proteins that play a role in the detection of [blank_start]DNA damage[blank_end], or DNA [blank_start]repair[blank_end]. This suggests that DNA damage plays a role in [blank_start]normal ageing[blank_end].
Answer
  • progeroid
  • mutations
  • DNA damage
  • repair
  • normal ageing

Question 21

Question
A [blank_start]mutation[blank_end] in the gene encoding nuclear A-type lamins has also been found in one [blank_start]progeroid[blank_end] syndrome, [blank_start]HGPS[blank_end]. [blank_start]Nuclear lamins[blank_end] are [blank_start]intermediate filaments proteins[blank_end], which form a structural lattice attached to the inner face of the [blank_start]nuclear envelope[blank_end] and play a role in cell [blank_start]division[blank_end] and gene [blank_start]expression[blank_end].
Answer
  • mutation
  • progeroid
  • HGPS
  • Nuclear lamins
  • intermediate filaments proteins
  • nuclear envelope
  • division
  • expression

Question 22

Question
The [blank_start]insulin/IGF-1-like[blank_end] signalling pathway in C. elegans , D. melanogaster and mice affects both [blank_start]stress responses[blank_end] and longevity. Activation of this pathway in these three laboratory model organisms leads to [blank_start]downregulation[blank_end] of stress response genes and [blank_start]reduces[blank_end] lifespan. Although an [blank_start]analogous[blank_end] pathway occurs in humans, and affects [blank_start]growth[blank_end] and metabolism, the effects on stress response genes and [blank_start]longevity[blank_end] are not known.
Answer
  • insulin/IGF-1-like
  • stress responses
  • downregulation
  • reduces
  • analogous
  • growth
  • longevity

Question 23

Question
mtDNA is more vulnerable to oxidative damage because:
Answer
  • mtDNA is not complexed with histones, which in nuclear chromatin, offer some protection against oxidative damage
  • almost all mtDNA is coding DNA, so any mutations that occur may affect gene products
  • DNA repair is not as efficient in the mitochondria, as not all DNA repair mechanisms take place
  • mtDNA is just more delicate than nuclear DNA

Question 24

Question
[blank_start]mtDNA[blank_end] codes for several [blank_start]proteins[blank_end] that are required in the [blank_start]TCA[blank_end] cycle and the [blank_start]electron transport[blank_end] chain. So if mtDNA is damaged by [blank_start]ROS[blank_end], this has huge repercussions on the cell's ability to [blank_start]generate energy[blank_end]. Combined with other age related damage to [blank_start]mitochondria[blank_end] in [blank_start]post-mitotic[blank_end] cells, to the membrane and proteins, this can be a real problem.
Answer
  • mtDNA
  • proteins
  • TCA
  • electron transport
  • ROS
  • generate energy
  • mitochondria
  • post-mitotic
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